The Impact of a Healthy Weight Intervention Embedded in a Home-Visiting Program on Children's Weight and Mothers’ Feeding Practices

Objective

To examine whether a healthy weight intervention embedded in the Parents as Teachers (PAT) home visiting program, which was previously found to improve mothers’ body mass index (BMI) and obesity-related behaviors, changed the BMI of preschool children or maternal feeding practices.

Sarcoidosis presenting with prolonged fever in a patient with sickle cell anemia.

Although the leading causes of fever and pulmonary infiltrates in sickle cell patients are acute bacterial pneumonia and the acute chest syndrome, the former is usually responsive to antibiotics and not protracted, and the clinical course of the latter is short and self-limited. A patient with sickle cell anemia presented with fever and pulmonary infiltrates of several weeks duration that were unresponsive to antibiotics. Gross endobronchial abnormalities were noted on bronchoscopy, and the biopsies were consistent with sarcoidosis. The diagnosis of sarcoidosis can be difficult to establish in a patient with sickle cell anemia and protracted fever since both disorders are associated with chronic interstitial changes on the chest radiograph as well as restrictive physiology.     

Learned changes of feeding behavior in Aplysia in response to edible and inedible foods

Feeding behavior in Aplysia fasciata and A. oculifera is modified by pairing the behavior with reinforcing consequences. Successful and unsuccessful attempts to transfer food from the buccal cavity to the crop act as positive and negative reinforcers, respectively. A number of changes in feeding behavior occur as a result of pairing of feeding with the negative reinforcer: feeding responses become less effective in leading to the entry of food into the buccal cavity; when food does enter the buccal cavity, it exits sooner; swallowing responses after food entry are less likely to occur; Aplysia eventually cease responding to food. Pairing successful transfer of food into the crop with feeding behavior produces opposite effects. Behavioral change is specific to pairing, as shown by lack of change when reinforcement is explicitly unpaired with feeding behavior. Behavioral change is specific to foods with a particular taste and texture; generalization to alternate foods was not observed. In spite of cessation of feeding, animals remain aroused, as shown by low response latency to alternate foods. Memory of response change persists for at least 48 hr.     

Development of cytochrome P-450-altered preneoplastic and neoplastic lesions during nitrosamine-induced hepatocarcinogenesis in the rat

The expression of four cytochrome (cyt.) P-450 isoenzymes has been studied in preneoplastic and neoplastic lesions during the course of nitrosamine-induced hepatocarcinogenesis in the female Wistar rat. Following exposure to diethylnitrosamine (50 or 100 ppm in the drinking water) for 10 days, animals were taken sequentially, and the livers were analyzed for the evolution of adenosine triphosphatase deficient focal lesions. These lesions were subdivided into different phenotypes with regard to their cyt. P-450 isoenzyme expression using serial frozen sections. Our results demonstrate that about 40% of the adenosine triphosphatase-deficient lesions show concomitant alterations in their cyt. P-450 isoenzyme contents. Of these lesions, islets which are characterized by decreased levels of at least three cyt. P-450 isoenzymes show a dramatic increase in their volumetric fraction of liver tissue with progression of time. Although only very few lesions express this phenotype, the contribution to the volumetric fraction of islet tissue raises from about 2% at 10 weeks to about 60% at 35 weeks after cessation of diethylnitrosamine treatment. By contrast, lesions which express less than two alterations in cyt. P-450 isoenzyme levels develop relatively slowly. Similar results were obtained when animals were exposed continuously to diethylnitrosamine for a period of up to 8 weeks. Following treatment of islet-bearing animals with phenobarbital, an induction of cyt. P-450 isoenzymes and NADPH-cyt. P-450-reductase was observed within preneoplastic and neoplastic lesions. This induction was most pronounced in large, expansively growing nodules, a type of lesion which displayed decreased levels of these enzymes in livers of animals not treated with phenobarbital. The elevation of the cyt. P-450 isoenzymes disappeared within 2 to 3 weeks after cessation of inducer treatment. Our results indicate that a high proportion of rapidly growing lesions has assumed a constitutive deficiency in cyt. P-450 isoenzyme expression during nitrosamine-induced hepatocarcinogenesis. This deficiency, however, is not an irreversible quality, since individual cyt. P-450 isoenzymes can be markedly induced by treatment with an enzyme inducer like phenobarbital. Thus, the observed decrease in cyt. P-450 expression during development of malignancy does not result from alterations in the cyt. P-450 encoding structural genes but may rather be related to abnormalities in the function of regulatory systems of a higher order which may play a central role in the maintenance of cell homeostasis.